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Review
. 2024 Sep 5;36(4):349-359.
doi: 10.4103/tcmj.tcmj_100_24. eCollection 2024 Oct-Dec.

Unraveling the interplay between inflammation and stem cell mobilization or homing: Implications for tissue repair and therapeutics

Hsin-Hou Chang  1 , Yu-Shan Liou  1 , Der-Shan Sun  1
Affiliations
Review

Unraveling the interplay between inflammation and stem cell mobilization or homing: Implications for tissue repair and therapeutics

Hsin-Hou Chang et al. Tzu Chi Med J. .

Abstract

Inflammation and stem cell mobilization or homing play pivotal roles in tissue repair and regeneration. This review explores their intricate interplay, elucidating their collaborative role in maintaining tissue homeostasis and responding to injury or disease. While examining the fundamentals of stem cells, we detail the mechanisms underlying inflammation, including immune cell recruitment and inflammatory mediator release, highlighting their self-renewal and differentiation capabilities. Central to our exploration is the modulation of hematopoietic stem cell behavior by inflammatory cues, driving their mobilization from the bone marrow niche into circulation. Key cytokines, chemokines, growth factors, and autophagy, an intracellular catabolic mechanism involved in this process, are discussed alongside their clinical relevance. Furthermore, mesenchymal stem cell homing in response to inflammation contributes to tissue repair processes. In addition, we discuss stem cell resilience in the face of inflammatory challenges. Moreover, we examine the reciprocal influence of stem cells on the inflammatory milieu, shaping immune responses and tissue repair. We underscore the potential of targeting inflammation-induced stem cell mobilization for regenerative therapies through extensive literature analysis and clinical insights. By unraveling the complex interplay between inflammation and stem cells, this review advances our understanding of tissue repair mechanisms and offers promising avenues for clinical translation in regenerative medicine.

Keywords: Inflammation; Resilience; Stem cell mobilization; Therapeutic interventions; Tissue regeneration.

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Conflict of interest statement

Dr. Hsin-Hou Chang, an editorial board member at the Tzu Chi Medical Journal, had no role in the peer review process or the decision to publish this article. The other authors declared no conflicts of interest in writing this article.

Figures

Figure 1
Figure 1
Schematic illustration showing the two types of inflammatory responses: injury-triggered and infection-triggered. Both inflammatory reactions involve recruiting immune cells to clear damaged cells or pathogens
Figure 2
Figure 2
Schematic illustration showing the activation pathway of the NLRP3 inflammasome. The NLRP3 inflammasome, a protein complex crucial for inflammation, involves NLRP3, ASC, and pro-caspase-1. Activation occurs in two steps: priming and activation. Priming involves pathogen-associated molecular patterns or damage-associated molecular patterns binding to toll-like receptors, activating the NF-κB pathway, and increasing pro-interleukin (IL)-1β, pro-IL-18, and NLRP3 expression. Activation involves ion flux, mitochondrial dysfunction, and lysosomal disruption, leading to the assembly of the inflammasome. Activated caspase-1 then cleaves pro-IL-1β, pro-IL-18, and gasdermin D, resulting in IL-1β and IL-18 secretion and pyroptosis
Figure 3
Figure 3
Schematic illustration showcasing mesenchymal stem cell (MSC) homing, depicting two pathways: nonsystemic homing and systemic homing. In nonsystemic homing, MSCs are injected locally near the target tissues. Conversely, MSCs navigate to the injury site or tumor in systemic homing through four subsequent steps: adhesion, facilitating rolling and capture, transendothelial migration, and homing to the injury site. In both modes of MSC homing, recruitment to the injury site is facilitated by the sensing of chemokines
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